Download Shock

Haemodynamics
in anaesthesia and intensive care
MUDr. Michal Horáček
Dept. of Anaesthesia/ICM
University Hospital Motol
Praha
Program
• circulation monitoring
• shock
• cannulations
• circulatory support
In part 1
• basic physiology
• heart rhythm disturbances
US Navy A central computer system monitors the heart rates
of each patient in the Intensive Care Unit of USN Hospital Ship 2002
• Monitoring = adjuncts and devices
• Clinical examination!
Clinical examination!
• heart rate, non-invasive blood pressure
– flow: CO = HR x SV
– perfusion pressure: MAP – CVP
– systemic vascular rezistence
• capillary blood flow:
– colour, temperature, cap. refill
•
•
•
•
cerebral blood flow = consciousness
renal blood flow = diuresis
oedemas?
piloerection?
How does blood pressure arise?
• heart
– stroke volume
– heart rate
– contractility
• vessel wall
– age
– aterosclerosis
– diabetes mellitus
• blood
– volume
– viscosity
Blood pressure and cardiac output
Ohm´s law: I (A) = U (V) /R (Ω)
Blood pressure and cardiac output
CO = (MPAP – LAP) / PVR
Blood pressure is not the same
everywhere!
Remember, where you measure!
Non-invasive
blood pressure
measurement
•
•
•
•
•
•
mercury sphygmomanometr
aneroid manometer (mechanical spring)
hybrid (electronic transducer instead of Hg )
oscilometry
aplanation tonometry
photopletysmography
Invasive blood pressure measurement
• hydraulic part
–
–
–
–
cannula or catheter
connecting tubes
taps
mechano-electrical transducer
• elektronic part
– pressure module/amplifier
– monitor
Blood pressure is not
only a number!
non-invasive method
invasive method
Pulsology
Stroke curve
anacrotic notch
volume component
dicrotic notch
inotropic
component
Changes of blood pressure
and stroke curve
towards periphery:
• SBP higher
• DBP lower
High pulse pressure
• Increased stroke volume
– hyperdynamic circulation
• anemia, AR, thyreotoxicosis, AV shunts, sepsis etc.
• Augmentation by reflected waves
– increased stiffness of central arteries
What can stroke wave tell us?
Functional haemodynamic
monitoring
• pressure changes during ventilation
• reaction to volume challenge
• reaction to
passive leg raising
Central venous pressure measurement
• curve description:
–
–
–
–
–
a = atrial contraction
c = tricuspid valve bulging
x = atrial relaxation, RV opening
v = atrial filling, tricusp. v. opening
y = RV filling
• normal values:
0-9 mm Hg = 0-12 cm H2O
• volume challenge
ac
x
v
y
Pulmonary (SG) catheter
Jeremy Swan
1922 - 2005
•
•
•
•
distal lumen
proximal lumen
cuff lumen
termistor
Vilém Ganz
1919-2009
SG insertion
Position check
What does SG catheter tell us?
• measurement • calculated parameters
– pressures:
•
•
•
•
RAP
RVP
PAP
PAWP
– cardiac output
• calculations
• samples
–
–
–
–
–
SVR/SVRI = (MAP-RAP)/CO, resp. CI
PVR/PVRI = (MPAP-PAWP)/CO, r. CI
stroke volume/index (SV/SI) = CO/HR
cardiac index (CI) = CO/BSA
left ventricle stroke work (LVSWI)
= (MAP – PAWP) . SV
– right ventricle stroke work (RVSWI)
= (MPAP – RAP) . SV
SG indications
Prof. Marco Ranucci
hemodynamically unstable patients:
• disturbed systolic function of left ventricle
• disturbed systolic function of right ventricle
• disturbed diastolic function of left ventricle
• Ventricular septum defect in AMI
• Mechanical support of left ventricle
Ranucci M. : Which cardiac surgical patients can benefit from placement
of a pulmonary artery catheter?
Crit´Care 2006;10 Suppl 3:S6.
Cardiac output measurement
• Fick´s method: Q = (VO2/(CA – CV))*100, NICO
• Finapres: Jan Peňáz 1967
• dilution method: Stewartova-Hamiltonova rce
– thermodilution
– dye dilution
– lithium dilution
•
•
•
•
echocardiography
sonography – oesophageal doppler
bioimpendance
stroke curve analysis: SV = 2 ml . pulse pressure
Cardiac output measurement
• thermodilution:
– intermitentní: classical pulmonary catheter
– continuous:
• Vigilance II Edwards Lifesciences
• Q2plus Hospira
– transpulmonal: PiCCO Pulsion Med. S.
• lithium dilution: LiDCO
• pulse wave analysis:
– calibrated: PiCCO, LiDCO
– self-calibrated: Flo/Trac Vigileo
– non-calibrated: Pressure Recording Analytical Method – MostCare,
Vytech
N Engl. J Med. 2001 Nov 8;345(19):1368-77.
• objem
• liberální x
konzervativní
přístup
(objem i DO2)
• dle potřeby
DO2
VO2
-15%
Echocardiography:
complete x focused examination
BEAT = Beat Index, Effusion,J Trauma.
Area, 2008;65:509
Tank –516
E
B
PLAX
PSAX
A4C
SC
A
A
T
Program
• circulation monitoring
• shock
• cannulation
• circulatory support
In part 1
• basic physiology
• heart rhythm disturbances
Shock = acute generalised decrease of flow
through metabolically active part of blood
circulation
Shock = global tissue hypoxia due to
imbalance between systemic DO2 / VO2
Van Beest et al.: Clinical review: use of venous oxygen saturations as a goal - a yet unfinished puzzle Critical Care 2011, 15:232
Shock
- pathophysiological classification
dr. Max Harry Weill
1927-2011
• hypovolemic
• cardiogennic
– obstructive
• distributive (vasogennic)
– anaphylactic
– septic
– neurogennic
Weil MH, Shubin H.: Proposed reclassification of shock states with special reference
to distributive defects Adv Exp Med Biol. 1971
Shock – time course
compensated shock: normal haemodynamics,
but redistribution and centralisation of blood →
microcirculatory disturbance (constriction of
precapillary sphincters, fluid mobilisation) →
insufficient tissue oxygenation
decomp. shock completed resuscitation:
static pressure parameters: TK, CVP, PAWP
– irreversible
microcirculatory statické volume parameters: EDV, GEDV
dynamic parameters: SPV, PPV, SVV
failure
metabolic parameters: SVO , lactate, BE
2
Shock organs
• shock myocardium
• shock lung:
V/Q disturbance → surfactant disturbance
→ instability of alveoli
• shock kidney:
hypoperfusion → intrarenal flow redistribution
→ diminished osmotic gradient → vessels
trombosins + tubular obstruction
• ischemia/reperfusion, apoptosis, MODS, death
Haemodynamic profiles
• PCWP, CO, SVR: low, normal, high
27 combinations
• hypovolemic: ↓ PCWP, ↓ CO, ↑ SVR
• cardiogennic: ↑ PCWP, ↓ CO, ↑ SVR
• vasogennic: ↓ PCWP, ↑ CO, ↓ SVR
Hemodynamic differentiation
1. Ascertain haemodynamic profile
e.g.: ↓ PCWP, ↓ CO, normal SVR
2. Ascertain problem
e.g.: hypovolemia, vasodilatation
3. Choose treatment
replenish volume and/or heart and SVR support
4. Underlying cause?
Hypovolemic shock
↓ PCWP, ↓ CO, ↑ SVR
• cause:
trauma, surgery, burns, diarrhea, vomiting, polyuria, sweating
• treatment:
– replenish volume according to need
– temporarily vazopressors to maintain perfusion pressures
• evaluation:
– macrocirculation: HR, BP, peripheral temperature, diuresis
– microcirculation: capillary refill, capillaroscopy
– biochemistry: ph, BE, lactate, SvO2
Life threatening bleeding (LTB)
•
•
•
•
•
•
blood volume 70 ml/kg adult, 85 ml/kg newborn
> 50 % blood volume
> 150 ml/min
> 1,5 ml/kg/min > 20 minutes
critical bleeding = LTB with massive transfusion
massive transfusion
– ½ blood volume during 4 hod (5 EM)
– > 1 blood volume in 24 hours
Trauma induced coagulopathy
• in 25% of patients
• acidosis + hypothermia
• endothelium
– thrombomodulin release → thrombin sequestration
→ APC production→ f. V a VIII inactivation =
anticoagulation
– tPA release → fibrinolysis
• volume replenishment → dilution of platelets
and coagulation factors
Treatment
• balanced resuscitation
– limited volume administered for maintaining organ perfusion
without disturbing haemostatické plug and worsening bleeding
• damage control resuscitation
–
–
–
–
–
–
lower than normal BP (permissive hypotension 80-100 mm Hg)
minimal volume resuscitation till bleeding stops
haemostatic transfusion of ERY, FFP, thrombo (1:1:<5)
coagulation factors (fibrinogen, kryoprecipitate, rfVIIa)
tranexamic acid (1 g i.v. in 10 min + 1 g i.v. during 8 hours)
surgery to stop bleeding and remove microbial contamination
Resuscitation targets in trauma patients
•
•
•
•
•
•
•
•
BP
80 mm Hg, MAP 50-60 mm Hg
HR
< 120/min
SaO2
> 96 % (and pulse oxymeter functioning)
diuresis > 0,5 ml/kg/hod
consciousnesss follows commands
lactate
< 1,6 mmol/l
BE
> -5 mmol/l
Hb
> 90 g/l
Nolan J.: Fluid resuscitation for the trauma patient. Resusc 2001;48:57-69
McCunn M, Dutton R. End-points of resuscitation: how much is enough?
Curr Opin Anaesthesiol 2000;13:147–53.
Cardiogennic shock
↑ PCWP, ↓ CO, ↑ SVR
• cause: function of hte heart as a pump decreases
– myogennic: infarction, cardiomyopathy, myocarditis, toxins
– mechanical: valve diseases, obstruction
– rythmogennic: tachy- / bradycardias
• most frequent: AMI (STEMI i non-STEMI), 5-10 % pt.
• ischemia → diastolic + systolic dysfunction → CO and
blood pressure decrease → DO2 decreases →
→ MODS → death
Cardiogennic shock treatment
• circulatory stabilisation:
– pharmacologic support:
• dobutamine, nitroglycerine, noradrenaline, levosimendan
– IABC, ECMO
• treatment of the cause:
– opening infarction artery = PCI
Acute coronary syndrome
• algic: unstable AP, non-STEMI, STEMI
• arrhythmic: sudden death, complex
ventricular dysrrhythmias
• congestive: diffuse coronary hypoperfusion
leading to heart failure
• combined
Unstable angina pectoris
• first presentation
• worsening pain:
–
–
–
–
more frequent
more intense
lasting longer
worsening reaction to nitrates
• rest pain
Obstructive shock
– pulmonary embolism
•
•
•
•
presentation: dyspnea + cough + haemoptysis
exams: D-dimers + echo + CT
heparine 5-10 000 u. i.v. + 1000 u./h - aPTT
thrombolysis:
unstable patients, shock, right heart failure
• thrombembolectomy
Obstructive shock - tamponade
• presentation:
– low BP
– high CVP
– still heart sounds
• diff. dg.
– hypovolemia
• treatment:
– pericardial puncture, surgery
Anaphylactic shock
↓ PCWP, ↑ CO, ↓ SVR
• severe, rapidly developing, life threatening generalised allergy
• cause:
– immunologic = reaction of Ag with antibody IgE
• degranulation of mastocytes a bazophiles → release:
• 1. histamine, proteases (tryptase, chymase) a heparine
• 2. NO (his), proinflammatory lipomediators (LT, TXA2, PAF)
• 3. additional chemo- and cytokines
• generalized inflammation
– non-immunologic (anaphylactoid) = non-IgE histamine relase,
mastocytosis
Anaphylactic shock
↓ PCWP, ↑ CO, ↓ SVR
allergy severity:
1. muco-cutaneous signs
2. muco-cutaneous signs + systemic signs
(hypotension, tachycardia, dyspnoa, GIT)
3. CV collaps ± muco-cutaneous signs
(tachy-/bradycardia, arrhythmias, hypotension,
bronchospasm, GIT)
4. circulatory arrest
Ring J, Messmer K: Incidence and severity of anaphylactoid reactions
to colloid volume substitutes. Lancet 1977; 1:466–9
Anaphylaktic shock
↓ PCWP, ↑ CO, ↓ SVR
1.
2.
3.
stop further antigen load and to stop anesthetics
maintain patent airways, 100% O2
restore circulation:
– adrenaline according to needs
(II. deg. 10-20 ug, III. deg.: 100-200 ug + inf 1-4 ug/min ,
IV. deg. CPR + 1-3 mg in 3 min + 3-5 mg in 3 min + inf. 4-10 ug/min)
– replenish volume using infusion (50% vol. given escapes)
– beta-2-mimetics
4. additional therapy:
–
corticoids, antihistamines
Septic shock - definiton
• infection
• SIRS (systemic inflammatory
response sy, ≥ 2 criteria)
Roger C. Bone
1941-1997
– temperature + tachycardia + tachypnoe + leukocytosis
• sepsis = infektion + SIRS
• severe sepsis = sepsis + organ dysfunction
– hypotension + change of consciousness + oliguria/creatinine
+ laktate ≥ 2 + Sa ≤ 90 % + hyperbili + thrombopenia
– diagnosis in max. 2 hours!
• septic shock = severe sepsis + hypotension despite
adequate volume resuscitation
Septic shock – treatment
Surviving Sepsis Campaign
Resuscitation bundle:
7 actions during 6 hours
•haemoculture
•lactate?
•ATB within 1 hours
•fluids = crystalloids
≥ 30 ml/kg for hypotension
•vazopressors: MAP ≥ 65
•CVP ≥ 8 mm Hg
•ScvO2 ≥ 70 %
• control of the infection
source (surgery/drainage)
Treatment bundle:
4 actions within 24 hours
• steroids in low dose?
• recomb. activ. protein C
(Xigris)
• glycemia < 8,3 mmol/l
• protective ventilation
Mortality
• hypovolemic: the lowest
• cardiogennic: 50-60 %
Herz 2011; 36:73–83
• sepsis:
– severe sepse 30-50 %
– septic shock : 70 %
– leading cause of death in non-coronary ICU
Program
• circulation monitoring
• shock
• cannulations
• circulatory support
In part 1
• basic physiology
• heart rhythm disturbances
sir Christopher Wren
1632-1723
Robert Aubaniac
Sven-Ivar Seldinger
Une nouvelle voie d’injection
1921-1998
ou de ponction veineuse:
1953
la voie sous-claviculaire.
Sem Hop Paris 1952; 28: 3445–3447
Venous access
pH
• dobutamine
• vancomycine
• naloxone
• SCHJ, cerucal
• frusemide
• thiopentone
• metohexital
• propofol
2,5-5,0
3,2
3,4
3,5
9,0
10,5
11,5
6-8,5
osmolalita (mosmol/l)
• F 1/1
• 5% glucoes
• 4% aminoacids
• 10% manitol
• 10% glucose
• 20% glucose
• 10% lipids
290
290
460
550
600
1250
280
Indications
•
•
•
•
•
•
immediate drug administration
drugs
infusion therapy – hydration, ion disturbances t.
parenteral nutrition
transfusion therapy
diagnostics
(measurement of pressures, blood drawing)
• treatment (extra-corporeal elimination, pacing etc.)
Sites of access
• peripheral veins incl. external jugular vein
• central veins
– subclavian vein
– internal jugular vein
– peripherally inserted central catheters PICC)
• intracardiac?
• intraosseal!
Indications of venous access
central vv.
• high volume
+
• highly effective drugs +
• irritating drugs
+
peripheral vv.
+
?
-
(osmo, pH)
•
•
•
•
long-term treatment
elimination methods
Swan-Ganz
Pacing
+
+
+
+
-
Cannulation
•
•
•
•
•
•
metal needle jehla
plastic cannula on the needle
Catheter through the needle
Seldinger´s method
Desillet-Hoffman´s method
implantable ports
Hagen-Poiseuille´s law
l
Q = flow, R = radius, µ = viscosity, dp/dx = pressure
change along the tube, l - length
Gauge, French a Charriere
• G = gauge = jauge (fr.) = měřidlo, míra
Stubs Iron Wire Gauge = Birmingham Wire Gauge
Gauge 1 = 0,3 inch (1 inch = 2.54 cm)
diameter (inch) = 0,3 x 0,897(gauge number – 1)
16 G = 1/16 inch x 2.54 (cm) = 1.58 mm
• French catheter scale
Joseph-Frédéric-Benoît Charrière
scale for sizes of urological catheters
1 F = 1 Charriere = 0.333 mm
• surgical sutures: American Wire Gauge
(1803–1876)
Comparison of cannulas
cannula
12 G
14 G
16 G
18 G
20 G
22 G
24 G
size (mm)
flow (ml/min)
2,1 * 45
1,7 * 45
1,3 * 45
1,1 * 40
330
215
97
55
36
18
Hagenův-Poiseuille´s law in practice
Size
• 24 G
• 22 G
• 20 G
ml/min
18
36
55
• 18 G
• 16 G
• 14 G
105
215
330
Central access
X
1 – subclavian v. infraclav.
1 - central catheters from
2 –subclavian v. supraclav.
periphery
3 – int. jugular v. posterior appr. 2 – „half-way“ catheters
4 – int. jugular v. central appr.
Subclavian vein infraclavicular
approach
Subclavian v.
Subclavian vein supraclavicular
approach
XX
X
X
Seldinger´s m.
Sterile insertion
Catheter insertion
18 F = 6 mm
7 F = 2,3 mm
Invasive measurement
of blood pressure
indications:
• fast changes of blood pressure
e.g. sepsis, bleeding, feochromocytoma
• vasoactive drugs
• large surgeries
• diagnostics, repeated blood samples
Sites for cannulation?
• superficially located
• collateral flow
• easy access
(puncture, care)
• minimal interference
•
•
•
•
•
•
•
•
a. radialis
a. femoralis
a. axillaris
a. cubitalis
a. brachialis
a. ulnaris
a. dorsalis pedis
a. temporalis spfc
Sites and cannulation methods
• Upper extremities
– a. radialis, ulnaris, brachialis, axillaris
• Lower extremities
– a. femoralis, tibialis post., dorsalis pedis
• direct puncture
• transfixion
• Seldinger´s technique
Arterial canulation procedure
• direct puncture
• transfixion
Program
• circulation monitoring
• shock
• cannulation
• circulatory support
In part 1
• basic physiology
• heart rhythm disturbances
Circulatory support to optimalize DO2
Oxygen delivery
Heart rate
Optimal heart rate
sinus rhythm 60-90/min
• distinguish: unstable x symptomatic
• treat underlying cause!
• slow down in tachycardias
– exclude compensatory tachycardia
– relieve other causes, e.g. pain, dyspnea, fever
– vagus, adenosine, betablockers, amiodarone, isoptin,
cardioversion
• speed up in bradycardias
– atropine
– beta-adrenergic drugs (dopamine, dobutamine, isoprenaline)
– cardiac pacing (transcutaneous, oesophageal, i.v., epicardial)
• secure synergy of contraction
– heart failure with QRS > 130 ms
Tachycardia Algorithm.
Neumar R W et al. Circulation 2010;122:S729-S767
Copyright © American Heart Association
Neumar R W et al. Circulation 2010;122:S729-S767
Copyright © American Heart Association
Contractility
Contractility
• myocardial function
independent of
preload and afterload
• dP/dT
echo
– systolic wall thickening
– RWMA
• hypo-, a-, dyskinesis
• factors:
– lenght of sarcomere
– Ca availibility
Calcium role in myocardial
contraction
Inotropics
• usual effect: ↑ iCa2+
–
–
–
–
β receptors → adenylatecyklase →↑cAMP →↑iCa2+
PDE III inhibitors →↑cAMP →↑iCa2+
α receptors → PLC → DAG → PKC → iCa2
Digoxine, istaroxime block Na/KATPase →↑Na/CaATPase
→↑iCa2+
• elevation of iCa2+
– ↑ demand for energy
– risk of heart rhythm disturbances ↑
– increase of mortality
Positive inotropic drugs
adrenergic
non-adrenergic
• katecholamines
•
•
•
•
•
•
•
•
•
–
–
–
–
–
adrenaline
dopamine
dobutamine
dopexamine
isoprenaline
• non-katecholamines
– ephedrine
– fenylefrine
– metoxamine
phosphodiesterase inhibitors
Bay K 8644
Ca
digoxine
forskoline
glucagon
levosimendan
naloxon
xantins
Beta receptors
phosphodiesterase
AMP
alfa-1 receptors
Levosimendan
• levo-simendan
• mechanism of effect
– ↑ afinity of troponin C to Ca
– inhibits PDE III
– opens KATP channels
• Clinical effect
– ↑ contractility
– vasodilatation (systémic, pulmonary, coronary)
– antiischaemic and antistunning effects
Vasopressin
• vasopressin = antidiuretic hormone
– diabetes insipidus
– sy of inadequate secretion
– circulation: vasoconstriction
• terlipressin
Circulatory support,
when drugs are not sufficient
• intra-aortic balloon counterpulsation
• resynchronisation therapy
• extracorporeal membrane oxygenation
Afterload
Afterload
• force acting against
myocardial fiber
shortening during
systole = wall stess
– vessel diameter
– vessel stiffness
– blood viskosity
• T = Pr/2h, TK, SVR
or PVR
If afterload increases?
• stroke volume
can be maintained
by incrreasing preload,
till its reserve is not
exhausted
Heart failure
• 1. phase
– preload increases (PCWP)
– „preload sensitive“
• 2. phase
– SV decreases, HR goes up
• 3. phase
– CO, SV go down,
preload and afterload
increase
– „afterload sensitive“
„Intensivist (and anaesthesiologist)
will always need
physiological knowledge
and with improving monitoring possibilities
the requirements on this knowledge
will be steadily increasing.“
prof. Jukka Takala, MD, PhD
in foreword to Invasive Haemodynamic Monitoring
Publisher Becton Dickinson UK Ltd, Oxford, UK, 2001